Binge and purge
Another article from Science Daily: “Gut bacteria can control organ functions,” which promises new directions for understanding of symbiotic relationships between animals and their commensal microorganisms. The research was very recently published in the online journal mBIO. In an article here on YCP-Micro from a few weeks ago, we learned about the relationship between gut microorganisms and sexual partner selection in fruit flies. In this article, we have moved a bit closer in the evolutionary tree, to an examination of the role of gut bacteria in mice, and their influence over metabolism of their host.
Mice were raised in germ-free conditions, without any of the microbiota that becomes associated with animals at birth. Germ free adult mice were then exposed to bedding that had been taken from mice with a normal microbial flora. The previously germ-free mice then acquired microbial flora from the bedding, and their gastrointestinal tracts rapidly became colonized with microorganisms. The researchers examined the mice over 20 days, but noticed that the mice very rapidly gained a significant amount of weight (4% weight gain) over the first five days. The microorganisms triggered alterations in liver function which enables the uptake and conversion of simple sugars such as glucose into glycogen and triglycerides for storage. This phenomenon seemed counter-intuitive to me at first; uptake and proliferation of microorganisms into the gut would lead to an increased biomass of those organisms, but they would be taking nutrients away from the host. This would seem then to lead to a loss of biomass from the host, and potential decrease in body weight as the colonization of the gut is established.
When the researchers characterized the bacteria found in the intestinal flora of these mice, one of the major groups of organisms were from the family Coriobacteriaceae, one of group of Gram positive rods which are among the most common terrestrial bacteria known. One family of these bacteria, the Streptomyces is a major source of antibiotics. The mechanism by which the Coriobacteriaceae modulate liver function in mice is as yet unknown, but it is possible that metabolites made by the microorganisms are having an effect on the liver. The hormone insulin accomplishes much the same thing as what these bacteria appear to be doing: causing the liver to upregulate the production of glycogen for storage of glucose. Whether the microorganisms are mimicking the action of insulin by stimulating glycogen synthase (the actual liver enzyme that is turned on by insulin) is not known, but it presumably would be rather easy to determine whether this is occurring. All BIO230 students will learn about this metabolic pathway (and it’s disorders) in excruciating detail when in A&P, so you are forewarned!
We have another excellent example of how symbiosis is somewhat more complicated than our first analysis might seem to indicate. There is an obvious benefit to the microbe for creating an environment conducive to maximize its potential growth rate. Also, we have a potential benefit to the host; the increase in size from the short term weight gain may lead to increased environmental fitness for the host, and maximize its ability to gather food for the microbiota. Will the reverse response occur if the microorganisms are lost from the gut suddenly? Is there a rapid weight loss, as glycogen shunts back to glucose, and body stores are depleted? Time may tell, but I’m not immediately ready to recommend the Coriobacteriaceae-free diet just yet.
BONUS: If the effect of weight gain is due to the presence of Coriobacteriaceae in the diet, how might we alter this in humans, without using an antibiotic?